Abstract

Scholars have long thought that bipedality evolved gradually in response to the opening of the savanna. Recently, both parts of this concept have come into question. A variety of benefits of bipedality have been posited as responsible, but a trait can not evolve unless a useful mutation appears. Perhaps we need to stop wondering about selective pressures and consider what kind of mutation might be involved in forming a bipedal pelvis. Work on the evolution of development has shown that there are segmental control genes, alterations in which have large effects. These include the hox genes, of which there are four sets in humans, referred to as the HOX A, B, C, and D sequences. Changes in their activation in embryogenesis alter the identity of vertebrae and limb structure. An alteration in the control region of certain of the distal HOX D genes may well be responsible for the sudden appearance of bipedality by moving the boundary between the lumbar and sacral vertebrae, and so moving the position of the pelvis and lower limb origin. Pongids usually have three lumbar vertebrae; early hominids, 6. Pongids also have 48 chromosomes while we have 46. HOX D is located on our 2nd chromosome, the one that is a fusion of two pongid chromosomes. If that fusion altered the onset of perhaps HOX D 10, so that it switched on a couple of segments later, then the sacrum would form further down the vertebral column and might be shorter. In this paper I look at the chromosomal location of HOX D and examine the likelihood that the fusion of two panid chromosomes could have given rise to alterations in its control resulting in the abrupt appearance of bipedality and accompanying changes in the limbs and in the chela in which the HOX sequences are reused.